Murine spleen culture: homing of hemopoietic progenitor cells to spleen is not mediated by a similar mechanism to that in marrow.

We have previously shown that in long-term bone marrow cultures (LTMC) the specific recognition and binding of hemopoietic stem cells to stroma, which we call "homing," is mediated by a recognition mechanism involving a surface membrane lectin with galactosyl and mannosyl specificities. Subsequent in vivo studies in lethally irradiated mice confirmed that homing to the marrow similarly involves a galactosyl- and mannosyl-specific recognition mechanism. However, these in vivo studies suggested that homing of hemopoietic progenitor cells to spleen was based upon a different molecular recognition mechanism. In the present study splenic homing was investigated in a cell culture system composed of an adherent layer of splenic stromal cells inoculated with stroma-free stem cells from the supernate of LTMC. In this system, splenic stroma supported proliferation and differentiation of hemopoietic precursors for a few weeks. When stem cells were added to the cultures in the presence or absence of inhibitory concentrations of neoglycoprotein reagents specific for galactosyl, mannosyl, or fucosyl lectins, the pattern of production of total cells, pluripotential stem cells (CFU-S), and granulocyte-macrophage committed progenitors (CFU-GM) remained the same. These data support our in vivo observations that homing of stem cells to splenic stroma is not mediated by a surface lectin with galactosyl and mannosyl specificities as it is in bone marrow, but rather by a different molecular mechanism.